2016 Fiscal Year Final Research Report
Role of cytidine deaminase in cell reprograming process
Project/Area Number |
26460363
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Research Category |
Grant-in-Aid for Scientific Research (C)
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Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
General medical chemistry
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Research Institution | Gifu University |
Principal Investigator |
Nagaoka Hitoshi 岐阜大学, 大学院医学系研究科, 教授 (20270647)
|
Project Period (FY) |
2014-04-01 – 2017-03-31
|
Keywords | 再生医学 / DNA脱メチル化 |
Outline of Final Research Achievements |
DNA methylation is one of the major epigenetic mark for gene regulation. Gene expression for DNA demethylation during iPS induction were evaluated. Consistent with previous reports, we failed to detect substantial expression of cytidine deaminases, AID and Apobec1 whereas Tet1 expression was significantly enhanced. Forced expression of AID or Apobec1 under the control of Nanog promoter exhibited no significant effect on iPS induction efficiency and stability at least until up to 60 days after induction. These results suggest minimum role of cytidine deaminases in iPS. These results suggest minimum role of cytidine deaminases in iPS. Hypomethylation at Aicda promoter region in iPS clones may indicate that leaky AID expression could easily occur under certain conditions in which appropriate transcription factors are available. That may explain apparently ambiguous reports for AID expression in iPS.
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Free Research Field |
分子生物学 分子免疫学
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